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Treatment Options for CoExisting Disorders and Understanding Recovery Dr. Phil O’Dwyer Brookfield Clinics Oakland University March 12, 2014 “The diagnosis should lead to the treatment plan which should lead to recovery” Q: What is meant by recovery? A: It all depends…. • Be Realistic: – Comorbid personality disorder and substance use disorder – Biochemical depression and substance use disorder – Lifelong challenges – Relapse v slip. It is an opportunity for learning and is not failure • Use a recovery perspective that is long term • Level of functioning and degree of disability matters • Consider a phased approach to treatment: – Engagement – Stabilization – Treatment – Aftercare • Distinguish between habilitation and rehabilitation • Address real life problems • Consider cognitive impairment when delivering treatment • Use support systems, technology • Understand the role of psychotropic medications Key Challenges • Finding integrated treatment programs for clients in the justice system • Jails are becoming surrogate mental hospitals • Youth and juvenile justice system experience substantially higher rates of mental disorders than the general population • At least 1 in 5 have a serious mental disorder • Adults have four times higher rates than the general population Psychopharmacology • Use Psychotherapy first…Better to not take medication • 50% of people recover from Depression with Psychotherapy alone (Stahl, 1996). • Meds. & Psychotherapy work well together. • Changes to one brain system or function will likely change something else that may or may not be known. Neurochemicals • Infants develop neural pathways at a terrific rate. • "The more scaffolds the greater the resilience of the brain" • When 2 neurons or more send messages to each other in a repetitive pattern a bond forms a pattern of neural connectivity or networks are established. • Thinking, remembering and learning are based on complex neural networks. Types of Neurotransmitters • • • • Acetylcholine (AC) Dopamine (D) Norepinephrine (N) Serotonin (S) • Glutamate (GL) • Gama-amino-butyric (GABA) • Histamine (H) • Glycine (GLY) GABA • Regulates brain activity balances excitation with inhibition • Anxious Patients have too little GABA • GABA agonists produce sedation, reduce anxiety – Xanax, Klonopin, etc… • GABA antagonists produce stimulation (counteract overdose of sedatives) Serotonin • Involved in emotional processing, mood, etc… • Depressed patients have too little Serotonin • SSRI’s prevent its reuptake • Prozac, Zoloft, Cymbalta, Pristiq, etc… Dopamine • Motor regulation, motivation, concentration, learning, etc… • Too little Dopamine – ADD, ADHD, Parkinson’s • Too much Dopamine – Schizophrenia, Delusional Dis., etc… • Dopamine Agonists – Meds for Parkinson’s – Ritalin, Adderall – “Cocaine” • Dopamine Antagonists – Risperdal, Geodon, Zyprexa Norepinephrine • Alertness, energy • Drives the fight or flight response • Too little = hypotension • Too much = hypertension The Agonist Spectrum When a drug binds to a receptor there are 5 reactions that can occur 1. The Full Agonist Effect – Opens the receptor – Xanax opens GABA receptors 2. The Partial Agonist Effect – Partially opens the receptor – Mild effects…Buspar 3. The Antagonist Effect – Blocks every other effect – Undoes agonists, etc… – Remeron, Nalaxone (Opiate o/d) – Antihistamines • Antagonists typically only block a current effect by blocking the receptor site The Agonist Spectrum 4. The Inverse Agonist Effect The exact opposite of the agonist Seeks to moderate an agonist effect Not many meds like this Flumazenil for Benzodiazepine o/d The Agonist Spectrum 5. Partial Inverse Agonist Mild version of inverse agonist Has mild action opposite of the agonist The Agonist Spectrum These 5 Effects -Occur naturally in the brain -Can be activated by medicine -All Psychotropic medications accomplish one of these effects Pharmokinetics What the Body does to Drugs • Absorbs, distributes, metabolizes and eliminates the drug. • Receptors adapt to a drug in the brain – It reduces the number of receptors which reduces the sensitivity to the drug – The brain “down regulates” • i.e. tolerance/dependence Barbiturates • CNS depressants that adjust brain functionality toward calming, restful feelings • In excess leads to coma • Highly addictive • They are glutamate antagonists – They produce sedation – Examples: Amytal, Nembutal, Seconal Benzodiazepines • Introduced 1960’s as anxiolytics, sedatives, anticonvulsants, relaxants • They are GABA agonists – i.e. the open GABA receptors that inhibit the neural activity causing anxiety for the client • 1st generation: Valium, Librium, Ativan, Klonopin, Xanax, Restoril • 2nd generation: Ambien, Buspar Antiepileptic Meds • Block repetitive firing of neurons • They enhance GABA’s ability to inhibit neural firing • Depakote, Neurontin, Lamectal Amphetamines • Mimic the action of adrenaline (epinephrine) • Designed to “upregulate” the brain • Stimulate the CNS by releasing Norepinephrine and dopamine from the pre-synaptic terminals • Motor skill, judgment and cognitive motivation run on dopamine • At low doses – increase BP, elevate mood, increase alertness and stimulate psychomotor activity Amphetamines (cont.) • “Upregulate” Norepinephrine and Dopamine to increase alertness • Methylphenidate is a Non-amphetamine Behavioral Stimulant – Increases dopamine by adjusting the balance of serotonin and dopamine in the brain. Antidepressants • Introduced in the 1960’s • Imiprimine – the first tricyclic antidepressant • 2nd generation 1980’s – Welbutrin, Desyral, Ascendin • 3rd generation 1990’s – SSRI’s • Consequences of untreated Depression Atypical Antipsychotic Meds • Schizophrenics need dopamine antagonists • Normalizing the dopamine transmission will improve thinking, improve motivation in ADHD, Parkinson’s, etc.. • Lack of Dopamine may cause the lack of motivation in depressed patients • Paranoid, aggressive, manic patients need Dopamine antagonists • Risperdal, Zyprexa, Seroquel, Geodon Addiction Risk • Meds have a role in balancing neurotransmitter systems in the brain • Patients need these meds to regulate their lives and behavior • Adverse side effects and substance abuse cause noncompliance • Relapse follows Addiction is a Disease caused by an “x-factor” - Circa 1950 The Disease concept is a myth - Fingarette 1988 Addiction is a learned behavior It results from lack of will power Addiction is a Brain Disease - 2000 How Do We Know? SPECT scans for 10 years can show the effects of addiction on the brain Currently more than 2,300 articles and scientific abstracts on Brain Imaging exist specifically for Psychiatry and Neurology Brain Scans Normal Brain is smooth, symmetrical and full; weight is 3 lbs Alcoholic Brain looks shriveled Marijuana Brain shows Temporal Lobe Deterioration Heroin Brain shows massive decreased activity throughout Cocaine Brain shows multiple small holes across the cerebral cortex Normal Brain Alcoholic Brain Normal Brain Marijuana Brain (underside view) Normal Brain Methamphetamine Brain Normal Brain Heroin Brain Do We Act Without Looking? Mental Health workers are the only health care professionals who rarely look at the organ they treat Rarely are brain scans conducted to see which areas are impaired Txs are presented based on client descriptions given over a very short period of time Why So Few SPECT Scans? Not good enough Not sophisticated enough Use multi-head SPECT scans not single-head Brain Imaging Studies Show: Physical changes in Drug Addicted patients Specific areas impaired are critical to: The reward system Memory Learning Decision-making Judgment, etc… How Does Addiction Occur? When a person performs an action that fulfills a desire, Dopamine is released into the Nucleus Acumbens and produces pleasure The Addicted Brain • The Nucleus Acumbens is a cluster of nerve cells below the cerebral hemisphere and is a key area in the Brain that drives the Reward System • In every pleasure of life a TRICKLE of Dopamine occurs in the Reward System (a joke, an orgasm, etc…) • Addictive Drugs FLOOD the Nucleus Acumbens “Candy is dandy but liquor is quicker” The Addicted Brain • The Brain can’t cope with the flood of Dopamine and post synaptic receptor sites begin to down-regulate • This results in: – Reduced natural capacity of the brain to produce Dopamine in the Reward pathway – Higher doses required and eventually the drug will have minimal pleasurable effects The Normal Brain A pleasurable event results in a large spike of Dopamine and then it quickly returns to normal The Addicted Brain Often has a higher set point (genetics) Drug high is more intense and longer Dopamine does not return to its normal baseline level, it plunges to zero This crash of Dopamine creates cravings to recreate the Dopamine surge The Amygdala stores the memory of every episode of “trickle” or “flooding” of Dopamine Then any stimulus that resembles either the “trickle” or the “flooding” event will trigger a conditioned response, a habit response and a repeated risk increases More jokes More orgasms More chemical use, etc… “Cells that fire together wire together” Addiction/repeated behaviors alter the strength of these pathways. The memory is triggered most powerfully by another dose of the drug The Amygdala Almond size and shape Part of the Limbic System Size related to level of aggression, sex Major Researchers of the Amygdala Ladoux – N.Y. University Davis – Emory University Amaral – University of Cal. Davis Cahill – University of Cal. Irvine Aggleton – Cardiff University